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Books on the topic 'Cancer grading'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 May 2024

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1

Damjanov, Ivan, and Fang Fan, eds. Cancer Grading Manual. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-34516-6.

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Damjanov, Ivan, and Fang Fan, eds. Cancer Grading Manual. Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-33751-7.

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3

Amin, Mahul B. Gleason grading of prostate cancer: A contemporary approach. Lippincott Williams & Wilkins, 2002.

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4

Brennan, Liam. Nucleolar organiser regions as a basis of cervical cancer grading. The Author], 1990.

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5

The Gleason grading system: A complete guide for pathologists and clinicians. Wolters Kluwer/Lippincott Williams & Wilkins Health, 2013.

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6

Mouriquand, Jacqueline. Diagnosis of non-palpable breast lesions: Ultrasonographically controlled fine-needle aspiration : diagnostic and prognostic implications of cytologic grading, morphometry, DNA cytometry, immunocytochemistry, and color doppler. Karger, 1993.

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7

Mouriquand, Jacqueline. Diagnosis of non-palpable breast lesions: Ultrasonographically controlled fine-needle aspirations : diagnostic and prognostic implications of cytologic grading, morphometry, DNA cytometry, immunocytochemistry, and color doppler. Karger, 1993.

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8

Damjanov, Ivan, and Fang Fan. Cancer Grading Manual. Springer, 2016.

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9

Damjanov, Ivan, and Fang Fan. Cancer Grading Manual. Springer, 2013.

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10

(Editor), Ivan Damjanov, and Fang Fan (Editor), eds. Cancer Grading Manual. Springer, 2006.

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11

Damjanov, Ivan, and Fang Fan. Cancer Grading Manual. Springer, 2007.

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12

Damjanov, Ivan, and Fang Fan. Cancer Grading Manual. Springer London, Limited, 2013.

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13

Pathological Staging and Grading of Cancer and Non-Cancer. Lulu Press, Inc., 2022.

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14

Gleason grading of prostate cancer: A contemporary approach. Lippincott Williams & Wilkins, 2004.

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15

Amin, Mahul B., David Grignon, Peter A. Humphrey, and John R. Srigley. Gleason Grading of Prostate Cancer: A Contemporary Approach. Lippincott Williams & Wilkins, 2003.

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16

Kroenke, Candyce, and Ichiro Kawachi. Socioeconomic Disparities in Cancer Incidence and Mortality. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0009.

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The relationship between socioeconomic status (SES) and cancer is complex, dynamic, and evolving. Associations depend on SES measures, cancer type, sociodemographic factors including race/ethnicity, and historical trends. However, socioeconomic disadvantage is often associated with a higher risk of cancer, particularly cancers diagnosed at a late stage, as well as worse prognosis once diagnosed. Research on secular trends over the past 70 years has shown reversals of the socioeconomic gradient for lung and colorectal cancer consistent with differential trends by SES in patterns of smoking, diet, and obesity. Rates of these cancers are now currently higher in socioeconomically disadvantaged groups. SES is considered to be a “fundamental” determinant of health outcomes, and this appears true throughout the cancer spectrum—from cancer incidence to detection, treatment, and survival. Investigations over the past decade have increasingly considered the simultaneous impact of individual SES and area-level SES (as a contextual influence) on health outcomes.

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17

Goodman, Steven N., and Jonathan M. Samet. Causal Inference in Cancer Epidemiology. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0007.

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Judgments about causality are central to the development of interventions intended to reduce exposure to risk factors that cause cancer. Because causation is not directly observable in medicine, scientists and philosophers have had to develop sets of constructs and heuristics that define “cause” operationally. The criteria in this framework, often attributed to the British medical statistician Sir Austin Bradford Hill or to the 1964 Report of the US Surgeon General on tobacco, include consistency, strength of association, specificity, temporality, coherence/plausibility/analogy, biological gradient, and experiment. This chapter reviews these criteria in depth and considers the challenges of applying them to population research on cancer. It discusses the concepts of causation in the context of the multistage nature of cancer, the “counterfactual” notion of causation, the component cause model for understanding diseases with multiple causes, and the “weight of the evidence” approach for integrating information from multiple lines of research.

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18

Gossai, Anala, Dorothea T. Barton, Judy R. Rees, Heather H. Nelson, and Margaret R. Karagas. Keratinocyte Cancers. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0058.

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Keratinocyte cancers (KC) include basal and squamous cell carcinomas that arise from keratinocytes or their precursors. KCs are the most common malignancies in humans. Basal cell carcinoma (BCC) has higher incidence rates, but squamous cell carcinoma (SCC) causes most deaths. Despite increasing incidence rates, the mortality rates have not changed markedly in recent years. The geographic and demographic features of these tumors have remained consistent over the past several decades, with a gradient of increasing incidence rates with proximity to the equator, predominantly affecting fair-skinned populations. Risk increases with age, is higher in men than women, and is associated with artificial as well as natural exposure to UV light. There is emerging evidence that these malignancies, particularly BCCs, may be increasing in younger adults and among women. While basal and squamous cell carcinomas share etiological factors, the relative importance of these factors, pattern of exposure, molecular alterations, and even the factors themselves differ.

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19

Gilbert, Mark R., and Roberta Rudà. Ependymal tumours. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0005.

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Ependymomas are uncommon central nervous system cancers that can arise in the supratentorial, infratentorial, or spinal cord region. Recently, there have been several seminal findings regarding the molecular profiles of ependymomas that have led to marked changes in the classification of this disease. In addition to the World Health Organization grading system that designates ependymomas based on histological appearance into grade I, II, or III, a new molecular classification with distinct entities within the three anatomical regions provides additional subtyping that has prognostic significance and may ultimately provide therapeutic targets. Ependymomas are typically treated with maximum safe tumour resection. Grade III tumours always require radiation treatment even with extensive resection. Radiation is also often administered to patients with grade II ependymomas. Grade I tumours typically receive radiation if there is extensive residual disease, but complete resection may be curative. Local radiation is optimal unless there is imaging or cytological evidence of dissemination in the cerebrospinal fluid. Chemotherapy is less well established although recent molecular findings may lead to subtype specific treatments.

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